LAUSR

Legumes can form symbiotic associations with rhizobia, which are nitrogen-fixing bacteria that colonize roots by forming facultative organs termed nodules. The development of nodules depends on a concerted interchange of signals between the plant and the symbiotic bacteria. Ultimately, legumes benefit from this association by being able to use nitrogen that would otherwise be unavailable, while rhizobia successfully multiply by utilizing plant resources mainly in the form of sugars (Oldroyd et al., 2011). The question remains, however, how plants distinguish these beneficial bacteria from bacteria that cause disease. Over a decade ago, research showed that some symbiotic bacteria could elicit the plant immune system by introducing specific proteins into host plants in a manner reminiscent of pathogenic bacteria (Deakin and Broughton, 2009). These proteins, known as nodulation outer proteins (Nops), can either induce nodulation or inhibit nodulation in a host-specific fashion, just as in the case of pathogen virulence and avirulence factors. Few plant proteins have been shown to interact directly or indirectly with Nops to trigger those responses and the mechanism of Nops action is poorly understood (Staehelin and Krishnan, 2015). In this issue of Plant Physiology, Khan and collaborators (2022) investigate the mode of action of NopT from Sinorhizobium (Ensifer) strain NGR234. This rhizobium strain can nodulate species from more than 100 plant genera (Pueppke and Broughton, 1999). NopT induces nodulation in strains of common bean (Phaseolus vulgaris) and negatively affects nodulation in the tropical legume Crotalaria pallida (Dai et al., 2008). Once in the plant, NopT cleaves itself to expose residues that become lipidated, activating a localization signal that directs NopT to the plasma membrane (Dowen et al., 2009). The authors first utilized a Xanthomonas (Xanthomonas campestris)–pepper (Capsicum annuum) translocation system to show that translocation of the NopT effector from NGR234 occurs through a bacterial type III secretion system (T3SS) and depends on NopT N-terminal residues. Further, with the use of a NGRDnopT mutant and by introducing plasmids with nopT mutations that lack specific residues, the authors corroborated that NopT requires lipidation and its protease activity to inhibit nodulation in C. pallida. To test the contribution of NopT in nodulation, the authors introduced nopT into Sinorhizobium fredii strain USDA257, which can induce nodulation in a wide range of soybean (Glycine max) accessions. The authors showed that nopT of NGR234 in the USDA257 strain inhibited nodulation of soybean cv. Nenfeng 15, indicating that NopT alone is sufficient to prevent symbiosis in some soybean accessions and when expressed in USDA257. Next, the authors investigated how NopT interferes with nodulation and their findings indicate that NopT triggers the plant defense pathway known as effector-triggered immunity (ETI). Plants have evolved an innate immune system that swiftly recognizes the majority of pathogens in their environment to mount a defensive response. In this innate immune system, a plant recognizes pathogen-associated molecular patterns to elicit a general response known as “pathogen triggered immunity” (PTI). In turn, some pathogens suppress PTI by secreting effectors, to which the plant may or may not be able to respond by triggering ETI, a second layer of response. ETI is strain-specific and characterized by hypersensitive response and programmed cell death at the site of infection, which effectively restrict pathogen proliferation (Jones and Dangl, 2006). NopT has sequence and structural homology with the avirulence factor AvrPphB from the pathogenic Pseudomonas N ew s an d V ie w s